Scientists discover why human muscles weaken with age – and one way to fight it

Researchers have uncovered a significant factor contributing to age-related muscle decline, identifying the gene DEAF1 as a key culprit. Their findings, published in "Proceedings of the National Academy of Sciences," reveal that as muscles age, the activity of the DEAF1 gene increases. This heightened activity leads to the overstimulation of a crucial cellular pathway known as mTORC1.

The mTORC1 pathway plays a vital role in regulating cell growth, protein production, and maintaining muscle mass. It allows muscles to respond to nutritional signals and exercise by increasing protein synthesis for building and repairing tissue. However, in aging muscles, the excessive activation of mTORC1, driven by DEAF1, disrupts this balance. While it promotes the production of new proteins, it simultaneously weakens the cell's ability to clear out damaged proteins. This accumulation of cellular debris impairs muscle function and leads to a loss of strength.

Experiments conducted on fruit flies and mice corroborated these findings. The researchers observed that increasing DEAF1 levels accelerated muscle weakening, while reducing its levels improved protein balance and muscle strength. This suggests that DEAF1's unchecked activity is a primary driver of sarcopenia, the age-related loss of muscle mass and function.

Encouragingly, the study also demonstrated that physical activity can partially reverse this process. Exercise triggers the production of proteins that lower DEAF1 levels, bringing the mTORC1 pathway closer to its normal activity. This supports the rebuilding of muscle tissue. The authors believe that understanding DEAF1's role could lead to new therapeutic strategies for protecting muscles in older adults and in patients experiencing muscle loss due to illness, surgery, or cancer treatment. They emphasize that maintaining strong muscles is essential not only for mobility but also for regulating metabolism.